KRAS and familial pancreatic carcinoma: Tumor cells took these lipids to support tumor growth.[78] TGF‐β, which could be up‐regulated by KRAS mutations, enhanced the transcription of fibrogenic factors in fibroblasts, and therefore contributed to collagen deposition.[79] Grunwald et al.[80] characterized the subtumor microenvironment (subTME) of pancreatic cancer, suggesting that certain pancreatic cancer patients exhibited intratumoral heterogeneity in their microenvironments.